What is “lacunar infarction”? How to deal with it?

"Lacunar cerebral infarction" is a small artery lesion blockage, which is an irregular tiny cavity left after the patient's brain ischemic infarction. It is mainly caused by diseases such as hypertension, diabetes and vasculitis. The disease can achieve ideal treatment effects after standardized and timely treatment, with low mortality and disability rates, but it is easy to have another infarction.

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1. Causes and inducing factors of lacunar infarction

"Lacunar cerebral infarction" is mainly caused by multiple factors acting on small arteries in the brain, such as hypertension, which can cause vascular wall hyaline degeneration, arteriosclerosis, and fibrous necrosis. Diabetes can cause abnormal vascular tissue structure. The narrowing of diseased small blood vessels and reduced blood flow are the basic causes of "lacunar cerebral infarction". Thrombosis and the detachment of tiny emboli blocking blood vessels will cause the originally narrowed blood vessels to become narrower and the blood flow to be further reduced. Basic diseases and lifestyle factors can induce "lacunar cerebral infarction". Hypertension is the most common cause of "lacunar cerebral infarction" and will increase the fragility of patients' blood vessels. Hyperlipidemia can increase the risk of atherosclerosis in patients. Diabetes can cause inflammation of small blood vessels. Sleep apnea symptoms can aggravate vascular wall lesions. Cardiovascular diseases such as heart failure and arrhythmia are prone to form cardiogenic emboli. The terminal arteries of deep perforating branches in the brain are the most common sites of "lacunar cerebral infarction". The infarction range is generally small and usually has multiple characteristics.

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2. What are the typical symptoms of “lacunar infarction”?

The typical symptoms of "lacunar infarction" are usually manifested as a variety of syndromes, including pure motor hemiparesis, dysarthria, pure sensory stroke, ataxic hemiparesis, etc. Pure motor hemiparesis is more common, and the embolism site is in the pons, internal capsule, corona radiata and other locations. After the lesion occurs, it has a great impact on the limbs and face on the hemiplegic side, but there will be no sensory, language and visual disorders. The infarction site of dysarthria is usually in the basal ganglia and internal capsule. After the onset of the disease, the patient will have difficulty in pronunciation and swallowing difficulties. At the same time, facial paralysis, hand weakness, fine motor disorders, etc. will occur on the opposite side of the lesion. Pure sensory stroke is more common, and the infarction site is in the ventral posterolateral nucleus of the thalamus. After the onset of the disease, the patient will have hemisensory disorders and paresthesias. The infarction site of ataxic hemiparesis is in the subcortical white matter, basal ganglia, and internal capsule. Mild hemiparesis is the main symptom, and the limbs on the hemiplegic side are ataxia, and the upper limbs are light and the lower limbs are heavy as the main manifestations.

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3. Rapid diagnosis of lacunar infarction

The treatment principle of "lacunar infarction" is early diagnosis and early treatment. Patients need to seek medical treatment in time for systematic and comprehensive examinations after the onset of symptoms related to "lacunar infarction", and actively treat after diagnosis. Usually, after patients find that they have limb movement disorders or sensory disorders, they need to seek medical treatment in time, accurately and truthfully describe their symptoms, and inform the doctor of their medical history. Doctors can accurately assess the patient's condition through physical examinations, symptom observations, etc. The doctor will determine whether the patient has a stroke, hemorrhagic or ischemic, whether it is a "lacunar infarction", the location and range of the lesion, and what the cause is. After the basic examination, in order to further clarify the diagnosis, doctors generally recommend that patients undergo imaging examinations, including CT, magnetic resonance imaging, carotid artery color ultrasound, cerebral angiography, echocardiography, etc.

4. How to treat lacunar infarction?

The treatment of "lacunar infarction" can be divided into general treatment, drug treatment, and surgical treatment. General treatment refers to the location of basic vital signs, treatment of underlying diseases, and prevention of further development of the disease. For patients who cannot breathe independently, tracheal intubation or incision should be carried out in time, airway support, oxygen inhalation, and unobstructed breathing should be given. Patients with hypertension and it is the main cause of the disease, and the patient's blood pressure needs to be slowly lowered and blood pressure should be closely monitored. Those with hypotension can be given appropriate blood volume expansion. If the patient's blood sugar level is relatively high, or if the patient is a confirmed diabetic, hypoglycemic treatment is required to maintain blood sugar stable and within the normal range. Patients with hypoglycemia are always given glucose oral solution or glucose is infused intravenously. Patients with high intracranial pressure use mannitol, glycerol fructose, etc. under the doctor's order to reduce intracranial pressure and prevent cerebral edema and brain herniation. For patients with dysphagia, nasogastric feeding or gastrostomy is established to form a nutritional pathway. If the patient has fever or infection, physical solutions such as ice caps and alcohol wiping the whole body can be used to cool down. Antibiotics should be used for patients as appropriate to prevent infection. Monitor the patient's water and electrolytes, provide targeted treatment, and correct the water and salt balance.

"Lacunar infarction" can be treated with drugs for thrombolysis, antiplatelet therapy, anticoagulant therapy, and defibrinolytic therapy. Thrombolytic therapy is the main means of clinical treatment of "lacunar infarction" at present, and urokinase and recombinant tissue plasminogen activator are commonly used. When thrombolytic therapy is used for patients with "lacunar infarction", the time window is very important. The effective time window for thrombolysis with urokinase is 6 hours, and the effective time window for thrombolysis with recombinant tissue plasminogen activator is 4.5 hours. On the basis of thrombolytic therapy for "lacunar infarction", aspirin, clopidogrel, etc. are needed for antiplatelet therapy to avoid platelet aggregation and re-thrombosis. If necessary, heparin, low molecular weight heparin, warfarin and other drugs are given for anticoagulant therapy, and the patient's coagulation status is closely monitored. Anticoagulant drugs are prohibited from being used within 24 hours of thrombolytic therapy, nor can they be used immediately after an acute attack. For patients with hyperfibrinemia, defibrase and batroxobin can be used after thrombolytic therapy. During the rehabilitation stage, patients need to be given drugs with neuroprotective effects, such as edaravone, citicoline, etc. Patients with severe conditions need timely surgical treatment, such as brainstem infarction or acute massive bleeding, and interventional treatment is the first choice.

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